The inflammatory response is a defense mechanism caused by various factors such as infection with pathogens or tissue injury and takes initial protective action to limit damage to an infected or injured area. In most cases, the inflammatory response leads to the removal of pathogenic factors and the induction of specific adaptive immunity by the components of innate immunity (Hawiger J., 2001). Redness, swelling, heat, pain, etc., known to be accompanied by inflammation, are the results of continuous inflammatory responses such as increased local blood flow and decreased local blood flow rate due to vasodilation caused by the action of inflammatory mediators and cytokines in the inflammation site, increased extravasation of plasma components due to increased permeability of blood vessels, increased extravasation of immune cells due to increased adhesion of vascular endothelial cells to circulating immune cells, and increased migration to the infected area by chemotaxis (Gallo R L, Murakami M, Takaaki O, Zaiou M., 2002; Graeme B. Ryan, M B, and Guido M., 1977).
Inflammation occurs in two phases. In the first phase, prostaglandins, leukotrienes (LT), etc. play an important role in the inflammatory response. That is, they induce strong chemotactic responses in leukocytes, which are also associated with the production of cytokines induced by Th1 (Maderna & Godson 2009). In the second phase, the production of lipid mediators, which actively control inflammation and promote the termination of inflammation, i.e., the resolution of inflammation, has recently been found.